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Steatohepatitis/Metabolic Liver Disease
Article first published online: 19 APR 2012
Copyright © 2012 American Association for the Study of Liver Diseases
Volume 55, Issue 5, pages 1406–1415, May 2012
How to Cite
Kozakova, M., Palombo, C., Paterni Eng, M., Dekker, J., Flyvbjerg, A., Mitrakou, A., Gastaldelli, A., Ferrannini, E. and ; and the RISC Investigators (2012), Fatty liver index, gamma-glutamyltransferase, and early carotid plaques. Hepatology, 55: 1406–1415. doi: 10.1002/hep.25555
Potential conflict of interest: Nothing to report.
The European Group for the Study of Insulin Resistance (EGIR) RISC study was partly supported by EU grant QLG1-CT-2001-01252. Additional support has been provided by AstraZeneca (Södertälje, Sweden). The EGIR is supported by Merck (Santé, France).
- Issue published online: 19 APR 2012
- Article first published online: 19 APR 2012
- Accepted manuscript online: 15 FEB 2012 04:09AM EST
- Manuscript Accepted: 28 NOV 2011
- Manuscript Received: 9 SEP 2011
An association between fatty liver and carotid atherosclerosis has been established; however, it is not clear whether this relationship is a consequence of shared conventional risk factors or whether it is determined by specific circulating factors originating from liver or adipose tissue. To identify the factors possibly linking fatty liver and atherosclerosis, we assessed, in 1,012 subjects free of confounding diseases (e.g., hypertension, diabetes, cardiovascular diseases, and dyslipidemia) and metabolic syndrome, the relationship between the presence of early plaques at carotid bifurcation and fatty liver index (FLI; a validated surrogate marker of fatty liver), as well as the associations between carotid plaque presence and established atherosclerotic risk factors, family history of cardiovascular disease (FH-CVD) or diabetes, insulin sensitivity, serum liver enzymes, adipokines, fatty free acids, and high-sensitivity C-reactive protein (hsCRP). A total of 55 of 1,012 subjects (5.4%) had small plaque at carotid bifurcation. Subjects with plaque were older and had higher prevalence of FLI ≥60 and FH-CVD, higher blood pressure, plasma low-density lipoprotein cholesterol, glucose, gamma-glutamyltransferase (GGT), and hsCRP, as compared to subjects without plaques (P < 0.05). In a logistic regression model, adjusted for sex, liver transaminase, and alcohol consumption, the independent predictors of plaque presence were age (P < 0.0005), FLI ≥60 (P < 0.0005), and current smoking (P < 0.05). When FLI in the model was replaced by variables used in its equation (e.g., body mass index, waist circumference, plasma triglycerides, and GGT), the independent determinants of plaque presence were age (P < 0.001), GGT (P = 0.001), and current smoking (P < 0.05). Conclusions: Our cross-sectional study suggests that subjects with FLI ≥60 are at higher risk of atherosclerotic lesions, independently of established risk factors, and that serum GGT may represent a link between fatty liver and the development of early atherosclerosis. (HEPATOLOGY 2012)